PMID: 19891703 鐥呮瘨铔嬬櫧 鈥濆钩琛♀滄矇榛橀斿緞
Plant J. 2009 Nov 3.
The Rice Yellow Mottle Virus P1 protein exhibits dual functions to suppress and activate gene silencing.聽聽 [涓嬭浇]
棰樼洰涓湁Rice锛屼絾骞朵笉鍙槸鍏充簬姘寸ɑ鐨勩
siRNA鏄按绋绘姉鐥呮瘨鐨勪竴绉嶅唴鍦ㄦ満鍒讹紝鐩稿簲鐨勶紝鐥呮瘨涔熶細浜х敓鎶戝埗瀛愭姷鎶楄繖绉嶆矇榛橀斿緞銆傛按绋婚粍鏂戦┏鐥呮瘨(RYMV)涓殑P1铔嬬櫧锛岄氳繃鍑忓皯21nt鎴栬24nt siRNA鐨勭Н绱(姣斿鍦ㄦ按绋讳腑锛屼富瑕佸奖鍝岲CL4閫斿緞)锛屽鍩哄洜娌夐粯鏈夐樆鎶戞晥搴(涓嶅悓鏉ユ簮鐨凱1铔嬬櫧鏁堝簲鏈夎緝澶у樊鍒)銆備笉杩囧湪鐑熻崏涓殑寮傛簮琛ㄨ揪鍙戠幇锛岃铔嬬櫧鍙嶈屼績杩涙矇榛樹俊鍙风殑浼犲銆傛渶鍚庤В閲婂埌杩欒泲鐧借捣涓涓濆钩琛♀滅殑浣滅敤锛岃鐥呮瘨灏藉绻佹畺鐨勫悓鏃朵篃涓瀹氱▼搴︿笂淇濇姢瀹夸富銆
鍡紝閫犵墿涓荤湡绁炲鈥︹
In plant, RNA silencing is a host defense mechanism against viral infection in which double strand RNA is processed into 21-24nt short interfering RNA (siRNA). Silencing spreads from cell-to-cell and systemically through a sequence-specific signal to limit the propagation of the virus. To counteract this defense mechanism, viruses encode suppressors of silencing. The P1 protein encoded by the Rice yellow mottle virus (RYMV) displays suppression activity with variable efficiency according to the isolates they originated from. Here, we show that P1 proteins from two RYMV isolates displaying contrasting suppression strength reduced local silencing induced by single strand and double strand RNA in Nicotiana benthamiana leaves. This suppression was associated with a slight and a severe reduction in 21nt and 24nt siRNA accumulation, respectively. Unexpectedly, cell-to-cell movement and systemic propagation of silencing were enhanced in P1 expressing Nicotiana plants. When transgenically expressed in rice, P1 proteins induced specific deregulation of DCL4-dependent endogenous siRNA pathways whereas the other endogenous pathways were not affected. Since DCL4-dependent pathways play a key role in rice development, expression of P1 viral proteins was associated to the same severe developmental defects in spikelets as in dcl4 mutants. Overall, our results demonstrate that a single viral protein display multiple effects on both endogenous and exogenous silencing not only in a suppressive but also in an enhancive manner. This suggests that P1 proteins play a key role in maintaining a subtle equilibrium between defense and counter-defense mechanisms to insure an efficient virus multiplication and the preservation of host integrity.

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